Porcine proliferative enteritis (PPE) is a major problem for the U.S. swine industry. PPE is an intestinal disease of pigs characterized by crypt hyperplasia and by the presence of intracellular campyiobacter-like organisms. Recognition of the disease has increased dramatically in the past ten years, with the incidence ranging as high as 20% and losses estimated at $50 million annually in the U.S. alone. Especially alarming is the apparent increase in incidence among the seed stock industry. The disease has been found world-wide and usually affects post-weanling pigs between six and twenty weeks of age. The clinical response of pigs affected with PPE includes intermittent diarrhea, anorexia, marked dullness and apathy, and a wasting syndrome. Death is not uncommon and is frequently associated with hemorrhage effect on intestines. Four different forms of the disease have been described, but the majority of the literature groups the lesions into two forms, acute and chronic, sometimes referred to as necrotic.
In the acute phase of the disease, macroscopic lesions are characterized by the presence of mesenteric and subserosal edema and pronounced reticulation of the serosa. The mucosa and muscle layers are thickened, with the mucosa forming deep longitudinal or transverse folds. The ridges of the folds are often hyperemic with some hemorrhage. Ulceration of the mucosa is occasionally evident with areas of viable mucosa adjacent to the lesion. At a microscopic level, acute lesions are characterized by an acute non-specific inflammation accompanied by hyperemia and edema in the lamina propria, by proliferation of epithelial cells, and by hypertrophy of the ileal musculature. The villi and intestinal crypt structure become irregular, with epithelial cell dysplasia. Crypt abscesses form as crypts become branched and fill with inflammatory cells. The villi and lamina propria become swollen due to the presence of edema and inflammatory cells. The submucosa usually contains lymphatic tissue nodules. The muscle of the ileum, especially the circular layers, may become hypertrophied.
In the chronic stage of the disease, macroscopic lesions are characterized by thickening of the lower small intestine. In some cases, inflammation and epithelial necrosis result in the formation of a fibrinous exudate. The mucosa frequently shows hyperemia and hemorrhage with occasional ulceration. The intestine is usually thickened throughout the lower small intestine, but the mucosal thickening is discontinuous, so that the mucosa is always thinner along the mesenteric attachment. Sometimes, the lumen contains a formed blood clot and the colon may contain tarry feces of mixed blood and digesta. The mucosal surface of the affected small intestine may show little gross damage except for the thickening. Erosions, bleeding points, and ulcers are usually not observed. In addition, the regional lymph nodes are markedly swollen. Microscopic lesions in the chronic stage are characterized by a transmural inflammatory reaction. The mucosa is more distorted with long irregular epithelioid projections. Crypts branch, and produce fissures in the mucosa at the borders of the hyperplastic areas. Ulcers may be seen. Crypt abscesses are also prominent in these areas. Intracellular bacteria, shaped as curved rods, are usually present in the crypt epithelium. The hyperplastic epithelial cells are columnar. Regenerative tissue contains irregularly-formed epithelial cells with a strongly basophilic cytoplasm. Goblet cells are usually infrequent in regeneration areas, but numerous in hyperplastic areas. The lamina propria shows abundant inflammatory cells. Granulomas are occasionally present in ulcerated areas. The submucosa contains dilated lymphatic vessels and fluid-filled tissue spaces. The muscle layers are hypertrophied, with alterations due to the presence of inflammatory cells and fibrin.
The presence of intracellular bacteria in the crypt epithelium of afflicted animals suggests a bacterial etiology for the disease. Although bacteria isolated from such animals are morphologically similar to Campylobacter spp, hybridization studies and reproduction experiments using various Campylobacter strains have demonstrated that this organism is not the etiological agent.
Effective PPE control measures have been limited. A basic trial-and-error therapeutic regimen which includes the use of oral and parenteral broad-spectrum antibiotics, antihistamines, corticosteroids, nitroimidazole, and B vitamins, usually becomes quite costly and typically proves ineffective. There has been limited success reproducing PPE using homogenates from affected ileum, and a number of infectious agents have been isolated from PPE-afflicted pigs, though none of these agents has been shown to reproduce the disease after controlled infection. Clearly, the isolation and characterization of the etiological agent of PPE would eliminate some of the trial and error therapeutic practices and would eventually lead to effective control measures using vaccination or medication.